Journal
JOURNAL OF PHARMACEUTICAL SCIENCES
Volume 100, Issue 9, Pages 3719-3730Publisher
ELSEVIER SCIENCE INC
DOI: 10.1002/jps.22614
Keywords
membrane transporter; solute transporters; phenotype; renal reabsorption intestinal secretion/transport; renal excretion
Funding
- Ministry of Education, Culture, Sports, Science, and Technology of Japan [19790585, 20390236]
- Grants-in-Aid for Scientific Research [23136511, 23689045, 22300262, 21790815, 23650480, 23591218, 23390226, 20390236, 19790585, 23617019] Funding Source: KAKEN
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Inorganic phosphate (Pi) is an essential physiological compound, highlighted by the syndromes caused by hypo or hyperphosphatemic states. Hyperphosphatemia is associated with ectopic calcification, cardiovascular disease, and increased mortality in patients with chronic kidney disease (CKD). As phosphate control is not efficient with diet or dialysis, oral Pi binders are used in over 90% of patients with renal failure. However, achieving tight control of serum Pi is difficult, and lower levels of serum Pi (severe hypophosphatemia) do not lead to better outcomes. The inhibition of sodium-dependent Pi (NaPi) transporter would be a preferable method to control serum Pi levels in patients with CKD or patients undergoing dialysis. Three types of NaPi transporters (types I-III) have been identified: solute carrier series SLC17A1 (NPT1/NaPi-I/OATv1), SLC34 (NaPi-IIa, NaPi-IIb, NaPi-IIc), and SLC20 (PiT1, PiT2), respectively. Knockout mice have been created for types I-III NaPi transporters. In this review, we discuss the roles of the NaPi transporters in Pi homeostasis. (C) 2011 Wiley-Liss, Inc. and the American Pharmacists Association J Pharm Sci 100:3719-3730, 2011
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